Artificial abnormal microenvironment caused by microperfusion of
L-glutamate (Glu) and Ca2+ in the hippocampus results in neuron damage, which is closely related to
cerebral ischemia.
Ginsenoside Rb1, a compound from Panax notoginseng, was previously used to counter the artificial abnormal hippocampal environment in a microperfusion model. In addition, while the Akt/mTOR/PTEN signaling pathway has been shown to mediate neuronprotection in
cerebral ischemia, whether this pathway is involved in the neuroprotection of
ginsenoside Rb1 is unknown. Here SH-SY5Y cells exposed to OGD/R injury in treated with
LY294002,
ginsenoside Rb1,
ginsenoside Rb1+ LY294002. Expressions of phosphorylation (P-)Akt/P-mTOR/P-PTEN (24 h after OGD/R) were detected by Western blotting. Effects were examined via the memory function of rats (by Morris water maze test), morphological changes in pyramidal cell (by histology), and
mRNA expression (by qRT-PCR) and phosphorylation (P-) (by Western blotting and immunohistochemical staining) of Akt, P-mTOR, and P-PTEN in the hippocampus. The
memory deficit of rats and pyramidal cellular
necrosis and apoptosis in the CA1 region of hippocampus after microperfusion of Glu and Ca2+ were dose dependently alleviated by
ginsenoside Rb1.Moreover,Western blot showed that
ginsenoside Rb1 increased the expressions of P-Akt, P-mTOR and reduced P-PTEN in vivo and vitro. Thus, the potent neuroprotection of
ginsenoside Rb1 in artificial abnormal microenvironment is, at least partially, related to the activation of P-AKT/P-mTOR signaling pathway and inhibition of P-
PTEN protein.